The long-term goal of this research is to determine the factors that mediate post-exercise hypotension and vasodilation. A single bout of aerobic exercise (e.g., cycling for 1 hour at a moderate level) produces a long-lasting decrease in blood pressure, known as "post-exercise hypotension." It is believed that post-exercise hypotension may play a role in the beneficial anti-hypertensive effects of endurance exercise training. Conversely, exaggerated post-exercise hypotension may result in a detrimental tendency to faint after exercise. Thus, there is a need to further understand what mediates post-exercise hypotension. Currently it is unknown whether the endogenous vasodilator nitric oxide contributes to this phenomenon. The specific goal of this study is to determine the role of the nitric oxide in post-exercise hypotension and vasodilation. The study plan is based on a randomized crossover design used previously to investigate post-exercise hypotension (Halliwill et al. J Physiol Lond 495:279-288, 1996). After a familiarization session and fitness test, subjects will undergo parallel experiments on two separate days. The order of the experiments will be randomized between sham, a 60 min period of seated upright rest: and exercise, a 60 min period of seated upright cycling at 60% of their peak aerobic power. Exercise of this intensity and duration produces a sustained (~2 hr) post-exercise hypotension (Halliwill et al. Am J. Physiol. 270:R420-R426, 1996). Following both sham and exercise, subjects will receive, in sequence, systemic alpha-adrenergic blockade (phentolamine) and nitric oxide synthase blockade (L-NMMA). Before and after these interventions, systemic and regional hemodynamics will be measured.